Objectives: Hwangryunhaedok-tang (HH) is a representative heat clearing multiherb prescription. We evaluated the protective effect of HH against heat stress exposure in mice. Methods: Six weeks old ICR mice were used for this study. After $43^{\circ}C$ heat stress for 15 minutes, we evaluated the changes of motor activity and c-fos expression level to determine the proper heat stress and evaluation time. The subjects were divided into 4 groups (1. control group, 2. heat stress group with normal saline, 3. heat stress group with administration of 100 mg/kg, and 4. heat stress group with administration of 1000 mg/kg). After oral administration of HH once a day for 3 days, 2, 3, 4 groups were exposed to $43^{\circ}C$ heat stress for 15 minutes. Then, we evaluated the motor activity for 120 minutes and analyzed the c-fos expression using western blot. We investigated the effect of HH and its ingredients on c-fos expressions after heat stress. The mice were administrated HH, Scutellariae Radix, Coptidis Rhizoma, Phellodendri Cortex, and Gardeniae Fructus for 3 days. After one hour of last treatment, the mice were exposed to heat stress at $43^{\circ}C$ for 15 min. After two hours, the hypothalamus was dissociated and lysed to measure c-fos expression. Results: After oral administration of HH for 3 days, motor activity was recovered insignificantly. 100 mg/kg HH treatment reduced the c-fos expression after heat stress but insignificantly. Among the ingredients of HH, Coptidis Rhizoma and Scutellariae Radix treatment groups significantly reduced the c-fos after stress. Conclusions: These results show that Hwangryunhaedok-tang may be effective to reduce the heat stress response.
Kim, So Young;Jeong, Mi Jin;Kim, Yoo Jin;Lee, Un-Tak;Choo, Sung-Tae;Kim, Mi Ryeo
The Korea Journal of Herbology
/
v.33
no.3
/
pp.63-70
/
2018
Objective : Previous studies showed that water extract of Plantago asiatica (Plantaginis asiaticae Folium, PAF) significantly controlled in body weights, adipose tissue weights and blood lipid profiles in obese C57BL/6 mice. To investigate the mechanism of anti-obesity action of PAF, expressions of obesity-related proteins were identified such as p-AMPK and p-ACC in hypothalamus, UCP-1 in brown adipose tissue, p-AMPK, p-ACC, SREBP-1c, $PPAR{\gamma}$, HMGCR and CPT-1 in liver. Method : Five-weeks old male C57BL/6 mice were divided into 5 groups; ND (normal diet + 0.9% saline), HFD (high-fat diet + 0.9% saline), PC (high-fat diet+Garcinia cambogia 500 mg/kg), PAF 100 and 300 (high-fat diet + PAF 100 or 300 mg/kg). PAF was treated orally for 6 weeks. The protein expression of AMPK, p-AMPK, ACC, p-ACC, $PPAR{\gamma}$, SREBP-1c, HMGCR, CPT-1 and UCP-1 were identified by expression levels of proteins through western blot analysis. Result : The results showed that protein expressions on hypothalamic p-AMPK and p-ACC did not differ between the HFD and PAF groups. In addition, PAF did not affect the increase of UCP-1 in brown adipose tissue. The protein expression levels of hepatic p-AMPK, p-ACC and CPT-1 increased in PAF groups compared to HFD group. And those of $PPAR{\gamma}$, SREBP-1c and HMG-CoA decreased in PAF groups compared to HFD group. Conclusion : These results suggest that the PAF administration induce weight loss via inhibition of lipid metabolism-related protein expressions in hepatic tissues. Therefore, PAF could be used as a potent material of anti-obesity products for prevention and treatment of obesity.
Suicide is a complex behavior associated with various neurobiological and psychosocial factors. It is considered that genetic polymorphism combined with environmental stress such as child-adolescent trauma make differences in neurobiological systems, which cause psychiatric disorders or pessimistic personality, impulse-aggressive behaviors, lack of judgment, and finally result in suicidal behavior. Much progress in the neurobiology of suicide has been made over the several decades. There seems to be a hereditary disposition to suicide independent of psychiatric disorder. The changes in neurotransmitters, neurohormones, neurotrophic factors, cytokines, lipid metabolisms related with their genetic polymorphism can contribute to disturbance of signal transductions and neuronal circuits vulnerable to suicide. It is likely that the main factors are dysfunctions of serotonin (5-HT) and hypothalamus-pituitary-adrenal (HPA) axis. Our understanding about the neurobiology of suicide is still limited. However, clinical practice could be assisted by neurobiological findings capable of making the detection of risk populations with higher sensitivity and the development of new treatment interventions. The settlement of biological markers in suicidal behaviors and their relationships is required.
Yoon Hee Choo;Moinay Kim;Jae Hyun Kim;Hanwool Jeon;Hee-Won Jung;Eun Jin Ha;Jiwoong Oh;Youngbo Shim;Seung Bin Kim;Han-Gil Jung;So Hee Park;Jung Ook Kim;Junhyung Kim;Hyeseon Kim;Seungjoo Lee
Journal of Korean Neurosurgical Society
/
v.66
no.6
/
pp.618-631
/
2023
The brain houses vital hormonal regulatory structures such as the hypothalamus and pituitary gland, which may confer unique susceptibilities to critical illness-related corticosteroid insufficiency (CIRCI) in patients with neurological disorders. In addition, the frequent use of steroids for therapeutic purposes in various neurological conditions may lead to the development of steroid insufficiency. This abstract aims to highlight the significance of understanding these relationships in the context of patient care and management for physicians. Neurological disorders may predispose patients to CIRCI due to the role of the brain in hormonal regulation. Early recognition of CIRCI in the context of neurological diseases is essential to ensure prompt and appropriate intervention. Moreover, the frequent use of steroids for treating neurological conditions can contribute to the development of steroid insufficiency, further complicating the clinical picture. Physicians must be aware of these unique interactions and be prepared to evaluate and manage patients with CIRCI and steroid insufficiency in the context of neurological disorders. This includes timely diagnosis, appropriate steroid administration, and careful monitoring for potential adverse effects. A comprehensive understanding of the interplay between neurological disease, CIRCI, and steroid insufficiency is critical for optimizing patient care and outcomes in this complex patient population.
Park, Song-Yi;Hwang, Jin-Taek;Lee, Yun-Kyoung;Kim, Young-Min;Park, Ock-Jin
Journal of Life Science
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v.19
no.4
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pp.423-428
/
2009
Selenium was investigated using human origin preadipocytes to see whether it possesses preventive or therapeutic effects for obesity. Unveiling the potential of selenium in the reduction of adipogenesis can help predict the therapeutic capabilities of selenium in obesity. In the present study, the molecular mechanism of the inhibition of adipogenesis by selenium was explored to unravel the involvement of the AMP-activated protein kinase. There is emerging evidence that AMPK, a sensor of cellular energy status, is a possible molecular target of controlling adipocyte differentiation on the basis of discovery that AMPK is responsible for the major metabolic responses to exercise, and integration of nutritional and hormonal signals to modulate feeding behavior or energy expenditure in the hypothalamus. Treatment of selenium resulted in inhibition of the adipocyte differentiation process and induction of mature apoptosis in 3T3-L1 adipocytes. We hypothesized that selenium may exert anti-adipogenic potential though modulating AMPK. We have found that selenium significantly activated AMPK and phosphorylated its substrate acetyl-CoA carboxylase ($ACC-serine^{79}$) during the inhibitory process of adipocytes. Also, the inhibition process of adipocyte differentiation by selenium was comparable to either reveratrol or a synthetic AMPK activator, AICAR (5-aminoimidazole-4-carboxamide-1-${\beta}$-D-ribofuranoside). To evaluate the involvement of AMPK in anti-lipogensis, we applied AICAR and Compound C, an AMPK inhibitor, to 3T3-L1-adipocytes and found that AMPK is required for the adipocyte differentiation blocking process. These results suggest that selenium has a potential to control adipogenesis and that this effect is mediated by AMPK, an essential kinase for both inhibition of adipocyte differentiation and apoptosis of mature adipocytes.
Objectives: The purpose of the present study is to investigate anti-depressive effects of Samul-tanggahyangbuja (SGH) on ovariectomized and chronic mild stress (CMS) induced rats. Methods: Ovariectomized rats were exposed to CMS for 4 weeks. Changes of depression behavior were tested by using sucrose intake test (SIT), elevated plus maze (EPM), forced swimming test (FST) and Morris water maze test (MWMT) in rats until being orally medicated with SGH (100 or 400 mg/kg/day). In addition, the serum levels of corticosterone (CORT), IL-4, IL-$1{\beta}$ and changes of 5-HT in the brain were measured. Results: 1. SGH 400 mg/kg treated group (SGH 400) significantly increased amount of sucrose intake compared with the control group (p<0.05). 2. SGH 100 mg/kg treated group (SGH 100) and SGH 400 significantly increased the time spent in the open arms of the EPM compared with the control group (p<0.01). SGH 400 also significantly increased the number of crossing of the open and closed arms compared with the control group (p<0.05). 3. SGH significantly shortened the immobility time in FST compared with the control group (SGH 100 p<0.05, SGH 400 p<0.01). 4. SGH significantly increased performance of acquisition trials compared with the control group (p<0.05, on day 4, 5 of SGH 100 and 400). SGH 400 also significantly increased performance of retention trials compared with the control group (p<0.05). 5. The serum levels of corticosterone and IL-4 were not significantly different among the groups. There were no changes on the serum levels of corticosterone, IL-$1{\beta}$ and IL-4 after administration with SGH. 6. SGH 400 significantly increased the level of 5-HT in the hippocampus compared with the control group (p<0.05). SGH significantly increased the levels of 5-HT in the hypothalamus compared with the control group (SGH 100 p<0.05, SGH 400 p<0.01). Conclusions: These results suggest that SGH has the anti-depressive effect on ovariectomized rat and affect 5-HT system rather than hypothalamic-pituitary-adrenal (HPA) axis and immune system.
Journal of the Korean Society of Food Science and Nutrition
/
v.31
no.5
/
pp.788-795
/
2002
This study described the effect of levan (9-2,6-linked fructose polymer) feeding on serum lipids, adiposity and uncoupling protein (UCP) expression in growing rats. Levan was synthesized from sucrose using bacterial levansucrase. UCP is a mitochondrial protein that uncouples the respiratory chain from oxidative Phosphorylation and generates heat instead of ATP, thereby increase energy expenditure. We observed that 3% or 5% levan containing diet reduced serum triglyceride levels, visceral and peritoneal fat mass and induced the UCP expression in rats fed high fat diet in previous study. To determine whether the intake of low level of levan may have the hypolipidemic and anti-obesity effect, 4 wk old Sprague Dawley male rats were fed AIN-76A diet for 6 wk, and sub-sequently fed 1% or 2% levan solution for further 5 wk. Intake of 1% levan in liquid form reduced serum triglyceride and serum total cholesterol levels to 50% and 66% of control group, respectively. Although epididymal and peritoneal fat masses were not affected by levan feeding, visceral fat mass was lower in 1% levan group compared to control group. The expression of UCP2 mRNA in brown adipose tissue, skeletal muscle and hypothalamus and UCP3 mRNA in skeletal muscle were not changed by levan feeding, while the UCP2 mRNA in white adipose tissue was up-regulated by levan feeding. In conclusions, intake of low level of levan solution reduced serum triglyceride and total cholesterol, restrained the visceral fat accumulation and increased UCP expression in white adipose tissue in rats. This study suggests that hypolipidemic and anti-obesity effect of levan attributed to anti-lipogenesis and inefficeint energy utilization by up-regulation of UCPs.
Nowadays, mongolian gerbil is widely utilized in the research of brain and water deprivation because of congenitally incomplete Willis' circle, audiogenic seizure in low noise, and special cholesterol metabolism without water absorption for a long time. In this study, we intended to identify the time lapse changes in the general morphoogy and ultrastructure of the catecholaminergic neurons of mongolian gerbil brain in after long-term water deprivation. Fifteen mongolian gerbils were divided into 3 groups (5, 10, and 20-day water deprivation groups), each with 5 mongolian gerbils. Additional 5 mongolian gerbils which received water without limitation were used as a control. The brain sections were immunostained using tyrosine hysroxylase (TH), $ dopamine-\beta-hydroxylase$ (DBH), and phenylethanolamine-N-methyltrasferase (PMNT) antibodies. And immunoreactive cells were observed by electromicroscopy for the ultrastructural changes . The TH-immunoreactive (TH-IR) nerve cells were observed in the para- and peri-ventricular nucleus of the 3 rd ventricle in the hypothalamus and the substantia nigra. The number of TH-IR neurons in these areas was decreased from the 5th day of the water deprivation to the 10 th day and reincreased until 20 th day water deprivation. The shape and density of the dopamine-secreting cells identified by immunohistochemistry showed changes in the continuous water deprivation. Electron microscopy revealed a round nucleus in the neurons of control group but 5-day water deprivation group showed a dense and irregularly shaped nucleus. Also in the 5-day water-deprived group, mitochondria was decreased in number and junctins were disappered. Endoplasmic reticulum, Golgi complex did not show changes after water-deprivation. In this results, we can conclude that dopamine are involved in the water metabolism in mongolian gerbil, and mongolian gerbil could be used as an animal model for the researches of water deprivation.
Kim, Jin-Hee;Lee, Kyoung-Ran;Kim, Hyeon-Kyeong;No, So-Hyeon;Yoo, Hye-Min;Moon, Chan-Il;Yang, Hyun-Won
Development and Reproduction
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v.15
no.4
/
pp.349-357
/
2011
Since nesfatin-1/NUCB2 involved in the control of appetite and energy metabolism was discovered for the first time in hypothalamus, many reports have shown its expression in various tissues. We also recently demonstrated that nesfatin-1/NUCB2 was expressed in the reproductive organs of mouse. However, no data exist on nesfatin-1/NUCB2 expression, regulation, and secretion in the uterus. Therefore, we examined the expression of nesfatin-1/NUCB2 in mouse uterus and the effects of PMSG and estrogen on its expression. NUCB2 mRNA expression in the uterus was determined by conventional and real-time PCR and nesfatin-1 protein expression was detected by western blotting. In immunohistochemistry staining, nesfatin-1 protein was localized at the epithelial cells of the uterine glands and endometrium. Nesfatin-1 protein binding sites were displayed at the epithelial cells of uterine glands and specific granulocytes including neutrophils. Additionally, to examine if the nesfatin-1/NUCB2 expression in the uterus is regulated by gonadotropin or estrogen, ovariectomized mice were treated with PMSG or $17{\beta}$-estradiol. The expression levels of NUCB2 mRNA in the uterus was significantly increased in the control mice after PMSG treatment, but not in the ovariectomized mice. In contrast, NUCB2 mRNA expression was dramatically increased in the ovariectomized mice after treatment with $17{\beta}$-estradiol. We report here for the first time that nesfatin-1/NUCB2 mRNA and protein express in the mouse uterus and its expression is regulated by estrogen secreted from the ovary, but not gonadotropin from the pituitary.
Ethane 1,2-dimethane sulfonate(EDS), a toxin which specifically kills Leydig cells(LC), has been widely used to prepare the reversible testosterone(T) depletion rat model. In the present study, we monitored the gene expression profiles of pituitary gonadotropins, LH and FSH, up to 7 weeks after EDS injection. Adult male Sprague-Dawley rats($300{\sim}350\;g$ B.W.) were injected with a single dose of EDS(75 mg/kg i.p.) and sacrificed on weeks 0, 1, 2, 3, 4, 5, 6 and 7. Total RNAs were purified from each pituitary, and the message levels of common alpha subunit($C{\alpha}$) of pituitary glycoprotein hormones, LH beta subunit($LH{\beta}$), FSH beta subunit($FSH{\beta}$) and GnRH receptor(GnRH-R) were evaluated by semi-quantitative RT-PCRs. The message levels of $C{\alpha}$ increased sharply during weeks 1-4, then return to the control level on week 5. The mRNA levels of $LH{\beta}$ were elevated after week 2, reached the peak at week 4, then declined to the control level after week 5. The message levels of $FSH{\beta}$ were elevated after week 2, reached the peak at week 3, then declined to the nadir at week 5. Similarly, the mRNA levels of GnRH-R were elevated after week 2, reached the peak at week 3, then gradually declined to the control level after week 5. The present study indicated that EDS treatment could induce reversible alterations in the transcriptional activities of gonadotropin subunits and GnRH-R in the anterior pituitary from male rats. EDS injection model might be useful to understand the mechanism of hormonal regulation of hypothalamus- pituitary neuroendocrine axis in male rats.
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